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Caspase-independent cell death

Jin L, Maeda T, Chandler WF, Uoyd RV (1993) Protein kinase C (PKC) activity and PKC messenger RNAs in human pituitary adenomas. Am J Pathol 142 569-578 Johnstone RW, Cretney E, Smyth MJ (1999) P-glycoprotein protects leukemia cells against caspase-dependent, but not caspase-independent, cell death. Blood 93 1075-1085... [Pg.76]

Mone AP, Cheney C, Banks AL et al. Alemtuzumab induces caspase-independent cell death in human chronic lymphocytic leukemia cells through a lipid raft-dependent mechanism. Leukemia... [Pg.227]

The other factor that may determine the type of cell death is the chemical structure of inducing agents [14]. We have recently found that u,(>-unsaluraled ketones such as 4,4-dimethyl-2-cyclopenten-l-one, a-methy-lene-y-butyrolactone, 5,6-dihydro-2H-pyran-2-one [15], codeinone [16], and morphinone [17] and a-hydroxylketones such as 3,3,3-trifluoro-2-hydroxy-1-phenyl-1-propanone induced caspase-independent cell death [18], induced vacuolization or autophagosome formation engulfing organelles, but without induction of apoptosis markers. [Pg.175]

Chi S, et al. Oncogenic Ras triggers cell suicide through the activation of a caspase-independent cell death program in human cancer cells. Oncogene 1999 18 2281-2290. [Pg.183]

Xu X, et al. Necrostatin-1 protects against glutamate-induced glutathione depletion and caspase-independent cell death in HT-22 cells. J. Neurochem. In press. [Pg.184]

Brocket LE, Huisman C, Span SW, Rodriguez JA, Kruyt FAE, Giaccone G (2004) Cathepsin B mediates caspase-independent cell death induced by microtubule stabilizing agents in nonsmall cell lung cancer cells. Cancer Res 64 27-30... [Pg.352]

Tuttolomondo A, Di Raimondo D, di Sciacca R, Pinto A, Licata G (2008) Inflammatory cytokines in acute ischemic stroke. CurrPharm Des 14 3574-3589 van Wijk SJ, Haegeman GJ (2005) Poly(ADP-ribose) polymeiase-1 mediated caspase-independent cell death after ischemia/reperfusion. Free Rad Biol Med 39 81-90 Walton M, Siiimanne E, Williams C, Gluckman P, Dragunow M (1996) The role of the cyclic AMP-responsive element binding protein (CREB) in hypoxic-ischemic brain damage and repair. Brain Res Mol Brain Res 43 21-29... [Pg.65]

Mohan J, Gandhi AA, Bhavya BC, Rashmi R, Karunagaran D, Indu R, Santhoskumar TR. 2006. Caspase-2 triggers Bax-Bak-dependent and -independent cell death in colon cancer cells treated with resveratrol. J Biol Chem 281 17599-17611. [Pg.356]

Kawahara A, et al. Caspase-independent cell killing by Fas-asso-ciated protein with death domain. J. Cell Biol. 1998 143 1353-1360. [Pg.183]

Holler, N., Zaru, R., Micheau, O., Thome, M., Attinger, A., Valitutti, S., Bodmer, J.L., Schneider, P., Seed, B., and Tschopp, J. (2000) Fas triggers an alternative, caspase-8-independent cell death pathway using the kinase RIP as effector molecule. Nat. Immunol., 1 489-495. [Pg.64]

Chan, H.T., Hughes, D., French, R.R., Tutt, A.L., Walshe, C.A., Peeling, J.L., Glennie, M.J., and Cragg, M.S., CD20-induced lymphoma cell death is independent of both caspases and its redistribution into triton X-100 insoluble membrane rafts. Cancer Res., 63, 5480-5489, 2003. [Pg.583]

Other Mechanisms Resveratrol activated caspase-2 and -8, resulting in the activation of downstream caspases, and induced cell death in a death receptor-or mitochondria-independent manner [Mohan et al., 2006]. The induction of apoptosis in HCT-116 (Bax+ / ) cells by resveratrol was mediated via activation of caspase 6 and subsequent degradation of nuclear coat protein lamin A [Lee et al., 2006]. Resveratrol induced a senescence-like growth arrest in HCT-116 cells via ROS-dependent activation of p38 MAP kinase and ATM kinase, and subsequent phosphorylation of p53 and induction of p21WAF1 CIP1 [Heiss et al., 2007]. In contrast, a p53-independent mechanism for resveratrol-induced apoptosis of HCT-116 cells was reported [Mahyar-Roemer et al., 2001, 2002]. [Pg.345]

Despite extensive research, identification of apoptotic cells remains an important unresolved issue. Apoptosis can be recognized by characteristic morphological features, which are difficult to be found in the heart. Furthermore, morphology alone does not enable recognition of cells early in the apoptotic pathway. Detection of activated caspases appears to be a reasonable way to detect apoptotic cells, given the central role of caspases in the process of apoptosis. It must be kept in mind, however, that caspases may contribute to necrotic cell death [80, 81] and caspase-independent apoptosis does occur [80]. [Pg.18]

Broker, L.E. et al. 2005. Cell death independent of caspases a review. Clin. Cancer Res. 11, 3155-3162. Bulanova, E.G. et al. 1995. Bioluminescent assay for human lymphocyte blast transformation. Immunol. Lett. 46, 153-155. [Pg.120]


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See also in sourсe #XX -- [ Pg.175 ]




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